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Last month's editorial offered a qualified endorsement of the pending Marketplace Fairness Act, which would subject online sales to sales tax. On the positive side, we noted the bill would [...]

Several letters to the editor are presented in response to the editorial published in the June 2013 issue focusing on the proposed legislation Marketplace Fairness Act which would subject online sales to sales tax in the U.S.

ABSTRACTHaemophilus ducreyiresists killing by antimicrobial peptides encountered during human infection, including cathelicidin LL-37, α-defensins, and β-defensins. In this study, we examined the role of the proton motive force-dependent multiple transferable resistance (MTR) transporter in antimicrobial peptide resistance in H. ducreyi. We found a proton motive force-dependent effect on H. ducreyi's resistance to LL-37 and β-defensin HBD-3, but not α-defensin HNP-2. Deletion of the membrane fusion protein MtrC rendered H. ducreyimore sensitive to LL-37 and human β-defensins but had relatively little effect on α-defensin resistance. The mtrCmutant 35000HPmtrCexhibited phenotypic changes in outer membrane protein profiles, colony morphology, and serum sensitivity, which were restored to wild type by trans-complementation with mtrC. Similar phenotypes were reported in a cpxAmutant; activation of the two-component CpxRA regulator was confirmed by showing transcriptional effects on CpxRA-regulated genes in 35000HPmtrC. A cpxRmutant had wild-type levels of antimicrobial peptide resistance; a cpxAmutation had little effect on defensin resistance but led to increased sensitivity to LL-37. 35000HPmtrCwas more sensitive than the cpxAmutant to LL-37, indicating that MTR contributed to LL-37 resistance independent of the CpxRA regulon. The CpxRA regulon did not affect proton motive force-dependent antimicrobial peptide resistance; however, 35000HPmtrChad lost proton motive force-dependent peptide resistance, suggesting that the MTR transporter promotes proton motive force-dependent resistance to LL-37 and human β-defensins. This is the first report of a β-defensin resistance mechanism in H. ducreyiand shows that LL-37 resistance in H. ducreyiis multifactorial.

OBJECTIVE: The Childhood Health Assessment Questionnaire (CHAQ) is a commonly used measure of disability and physical function for children with juvenile rheumatoid arthritis (JRA), whose scores range between 0 (no disability) and 3 (very severe disability), with a smallest potential difference in the CHAQ score of individuals at 0.125. We estimated minimal clinically important differences (MCID) of the CHAQ for worsening and improvement that were actually experienced by children with JRA using patient, parent, and clinical perspectives. METHODS: Changes in CHAQ scores were calculated for parent (n = 92) and patient ratings (children age ≥ 8 yrs only; n = 67) between subsequent clinic visits. Changes in patient well being and disease activity and the occurrence of flare or important improvement between visits served as external standards for the MCID. MCID were defined as the median changes of the CHAQ scores of individual patients who had a minimal important improvement or worsening between visits. RESULTS: The median change in CHAQ scores of patients who rated themselves or were rated by others as unchanged was often 0. Depending on the external standard used, the MCID for improvement of the CHAQ was –0.188 at most, while the MCID for worsening was at most +0.125. CONCLUSION: The MCID of the CHAQ for both improvement and worsening are often at or close to the level of the smallest potential difference, suggesting that the CHAQ is relatively insensitive to important short term changes in children with JRA. This may warrant a change in the calculation of the global CHAQ score, or the development of more sensitive functional measures.

Lens regeneration in vivo is restricted to some urodeles only. After removal of the lens, this remarkable event is initiated from the dorsal iris. The pigmented epithelial cells from the dorsal iris dedifferentiate and subsequently transdifferentiate to form the regenerating lens. This property of the dorsal iris implies specific regulation along the dorsal-ventral axis. To date, no known genes are known to be specifically expressed in the dedifferentiating cells and to be involved in lens regeneration. In this paper, we show that FGFR-1 expression and function is correlated with the process of lens regeneration from the dorsal iris. Following lentectomy, FGFR-1 protein is specifically present in the dedifferentiating pigment epithelial cells in the dorsal iris, but is absent from the ventral iris. Subsequently, FGFR-1 protein is present throughout the process of lens regeneration and fiber differentiation. Furthermore, we show that an FGFR-1-specific inhibitor is able to inhibit the process of transdifferentiation and lens regeneration. In this sense, FGFR-1 can be regarded as the first known lens regeneration-associated factor. Dev. Dyn. 1998;213:140–146. © 1998 Wiley-Liss, Inc.